human crc cell line ht29  (ATCC)


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    Structured Review

    ATCC human crc cell line ht29
    Chloroquine inhibits the migration, viability and colony formation of <t>HT29</t> cells by inhibiting TLR9. Chloroquine (15 and 25 µg/ml) inhibited the migration of HT29 cells in a dose-dependent manner at 48 h compared with the control group, which was determined using a wound healing assay. (A) Representative images were photographed (magnification ×100) and (B) migration rates were calculated. Proliferation rate of HT29 cells was reduced by chloroquine treatment (15 and 25 µg/ml), which was determined using a colony formation assay. (C) Representative images were photographed and (D) the relative colony number was analyzed. *P
    Human Crc Cell Line Ht29, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human crc cell line ht29/product/ATCC
    Average 99 stars, based on 9 article reviews
    Price from $9.99 to $1999.99
    human crc cell line ht29 - by Bioz Stars, 2022-11
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    Images

    1) Product Images from "TLR9 induces colitis-associated colorectal carcinogenesis by regulating NF-κB expression levels"

    Article Title: TLR9 induces colitis-associated colorectal carcinogenesis by regulating NF-κB expression levels

    Journal: Oncology Letters

    doi: 10.3892/ol.2020.11971

    Chloroquine inhibits the migration, viability and colony formation of HT29 cells by inhibiting TLR9. Chloroquine (15 and 25 µg/ml) inhibited the migration of HT29 cells in a dose-dependent manner at 48 h compared with the control group, which was determined using a wound healing assay. (A) Representative images were photographed (magnification ×100) and (B) migration rates were calculated. Proliferation rate of HT29 cells was reduced by chloroquine treatment (15 and 25 µg/ml), which was determined using a colony formation assay. (C) Representative images were photographed and (D) the relative colony number was analyzed. *P
    Figure Legend Snippet: Chloroquine inhibits the migration, viability and colony formation of HT29 cells by inhibiting TLR9. Chloroquine (15 and 25 µg/ml) inhibited the migration of HT29 cells in a dose-dependent manner at 48 h compared with the control group, which was determined using a wound healing assay. (A) Representative images were photographed (magnification ×100) and (B) migration rates were calculated. Proliferation rate of HT29 cells was reduced by chloroquine treatment (15 and 25 µg/ml), which was determined using a colony formation assay. (C) Representative images were photographed and (D) the relative colony number was analyzed. *P

    Techniques Used: Migration, Wound Healing Assay, Colony Assay

    2) Product Images from "IL-33 facilitates proliferation of colorectal cancer dependent on COX2/PGE2"

    Article Title: IL-33 facilitates proliferation of colorectal cancer dependent on COX2/PGE2

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    doi: 10.1186/s13046-018-0839-7

    IL-33/ST2 upregulates COX2 expression through NF-κB signaling. a , b The COX2 mRNA ( a ) and protein ( b ) expression in primary CRC cells or HT29 cells responding to the incubation with rhIL33 (100 ng/mL) or/ and ST2 antibody (2 μg/mL) for 24 h. Each experiment was performed three times. Data expressed as mean ± SEM. ** P
    Figure Legend Snippet: IL-33/ST2 upregulates COX2 expression through NF-κB signaling. a , b The COX2 mRNA ( a ) and protein ( b ) expression in primary CRC cells or HT29 cells responding to the incubation with rhIL33 (100 ng/mL) or/ and ST2 antibody (2 μg/mL) for 24 h. Each experiment was performed three times. Data expressed as mean ± SEM. ** P

    Techniques Used: Expressing, Incubation

    3) Product Images from "IL-33 facilitates proliferation of colorectal cancer dependent on COX2/PGE2"

    Article Title: IL-33 facilitates proliferation of colorectal cancer dependent on COX2/PGE2

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    doi: 10.1186/s13046-018-0839-7

    IL-33/ST2 upregulates COX2 expression through NF-κB signaling. a , b The COX2 mRNA ( a ) and protein ( b ) expression in primary CRC cells or HT29 cells responding to the incubation with rhIL33 (100 ng/mL) or/ and ST2 antibody (2 μg/mL) for 24 h. Each experiment was performed three times. Data expressed as mean ± SEM. ** P
    Figure Legend Snippet: IL-33/ST2 upregulates COX2 expression through NF-κB signaling. a , b The COX2 mRNA ( a ) and protein ( b ) expression in primary CRC cells or HT29 cells responding to the incubation with rhIL33 (100 ng/mL) or/ and ST2 antibody (2 μg/mL) for 24 h. Each experiment was performed three times. Data expressed as mean ± SEM. ** P

    Techniques Used: Expressing, Incubation

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    ATCC human crc cell lines
    Transcriptional factor III A mediates epithelial-mesenchymal transition of colorectal cancer <t>cells</t> by regulating cystatin A. A: Epithelial-mesenchymal transition (EMT) biomarkers E-cadherin, beta-catenin, and snail in short hairpin of transcriptional factor III A (shGTF3A) #1 and <t>#4-HCT116</t> cells and the control group were detected by Western blot; B: EMT biomarkers were tested in shGTF3A#1 and <t>#4-SW480</t> cells and the control group; C: mRNA expression of cystatin A ( Csta ) gene in shCSTA#1,2-SW480 and the control group was detected using real-time quantitative polymerase chain reaction; D: EMT biomarkers were analyzed in Csta -knockdown SW480 and the control cells. Cystatin A mRNA expression is expressed as the mean ± SEM of three independent experiments. There were statistically significant differences between shCSTA#1,2-SW480 and the control group. c P
    Human Crc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 1 article reviews
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    ATCC crc cell lines
    MiR-663b can reverse the inhibitive effects of circ_0003215 in <t>CRC</t> cells. A Correlation analysis between the expression levels of circ_0003215 and miR-663b expression. B FISH analysis of circ_0003215(red) and miR-663b(green) in <t>HT29</t> cells transfected with empty vector or circ_0003215 plasmid. C , D CCK8 and EdU analysis of the proliferation capacities in HT29 or <t>SW480</t> cells with diferent transfection. E Colony formation assay of HT29 or SW480 cells transfected with diferent transfection F Wound healing assay to evaluate the <t>cell</t> migration of HT29 cells with diferent transfection. G , H Transwell assay for the invasion and migration ability of CRC cells transfected with indicated vectors. Graph represents mean ± SD; * P
    Crc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human crc cell lines ht29
    The function of GAS6-AS1 is mediated by miR-370-3p and miR-1296-5p. A – E miR-370-3p and miR-1296-5p mimics suppressed the proliferation, migration and invasion of <t>HT29</t> <t>cells,</t> whereas miR-370-3p and miR-1296-5p mimics partially offset the promotion effects of GAS6-AS1 on HT29 cells’ proliferation, migration and invasion. F – J miR-370-3p and miR-1296-5p inhibitors promoted the proliferation, migration and invasion of LoVo cells, whereas miR-370-3p and miR-1296-5p inhibitors partially reversed the inhibitory effects of shGAS6-AS1 on LoVo cells’ proliferation, migration and invasion. ** P
    Human Crc Cell Lines Ht29, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human crc cell lines ht29/product/ATCC
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    human crc cell lines ht29 - by Bioz Stars, 2022-11
    99/100 stars
      Buy from Supplier

    Image Search Results


    Transcriptional factor III A mediates epithelial-mesenchymal transition of colorectal cancer cells by regulating cystatin A. A: Epithelial-mesenchymal transition (EMT) biomarkers E-cadherin, beta-catenin, and snail in short hairpin of transcriptional factor III A (shGTF3A) #1 and #4-HCT116 cells and the control group were detected by Western blot; B: EMT biomarkers were tested in shGTF3A#1 and #4-SW480 cells and the control group; C: mRNA expression of cystatin A ( Csta ) gene in shCSTA#1,2-SW480 and the control group was detected using real-time quantitative polymerase chain reaction; D: EMT biomarkers were analyzed in Csta -knockdown SW480 and the control cells. Cystatin A mRNA expression is expressed as the mean ± SEM of three independent experiments. There were statistically significant differences between shCSTA#1,2-SW480 and the control group. c P

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: Transcriptional factor III A promotes colorectal cancer progression by upregulating cystatin A

    doi: 10.4251/wjgo.v14.i10.1918

    Figure Lengend Snippet: Transcriptional factor III A mediates epithelial-mesenchymal transition of colorectal cancer cells by regulating cystatin A. A: Epithelial-mesenchymal transition (EMT) biomarkers E-cadherin, beta-catenin, and snail in short hairpin of transcriptional factor III A (shGTF3A) #1 and #4-HCT116 cells and the control group were detected by Western blot; B: EMT biomarkers were tested in shGTF3A#1 and #4-SW480 cells and the control group; C: mRNA expression of cystatin A ( Csta ) gene in shCSTA#1,2-SW480 and the control group was detected using real-time quantitative polymerase chain reaction; D: EMT biomarkers were analyzed in Csta -knockdown SW480 and the control cells. Cystatin A mRNA expression is expressed as the mean ± SEM of three independent experiments. There were statistically significant differences between shCSTA#1,2-SW480 and the control group. c P

    Article Snippet: Human CRC cell lines (HCT116, SW480, DLD1, SW620, and HT29) were obtained from the American Type Culture Collection (Manassas, VA, United States) and were purchased from the Shanghai Cell Center (Shanghai, China).

    Techniques: Western Blot, Expressing, Real-time Polymerase Chain Reaction

    Knockdown of transcriptional factor III A gene inhibits colorectal cancer cell proliferation. A: The expression of transcriptional factor III A (GTF3A) in HCT116, SW480, DLD-1, SW620, and HT-29 cells was detected by Western blot; B: HCT116 and SW480 cells were stably transfected with short hairpin (sh) shscramble and shGTF3A#1 and #4-GV112 virus, respectively. Gtf3a mRNA (b1) and GTF3A protein (b2) expression were detected using real-time quantitative polymerase chain reaction and Western blot, respectively. The cell viability of HCT116 and SW480-shscramble as well as shGTF3A#1 and #4 cells was detected using Cell Counting Kit assay (b3); C: Colony formation of the transfected HCT116 and SW480 cells was detected using colony formation assay (c1), and the colony number was counted (c2). Gtf3a mRNA expression, cell colony number, and cell viability are expressed as the mean ± SEM of three independent experiments. a P

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: Transcriptional factor III A promotes colorectal cancer progression by upregulating cystatin A

    doi: 10.4251/wjgo.v14.i10.1918

    Figure Lengend Snippet: Knockdown of transcriptional factor III A gene inhibits colorectal cancer cell proliferation. A: The expression of transcriptional factor III A (GTF3A) in HCT116, SW480, DLD-1, SW620, and HT-29 cells was detected by Western blot; B: HCT116 and SW480 cells were stably transfected with short hairpin (sh) shscramble and shGTF3A#1 and #4-GV112 virus, respectively. Gtf3a mRNA (b1) and GTF3A protein (b2) expression were detected using real-time quantitative polymerase chain reaction and Western blot, respectively. The cell viability of HCT116 and SW480-shscramble as well as shGTF3A#1 and #4 cells was detected using Cell Counting Kit assay (b3); C: Colony formation of the transfected HCT116 and SW480 cells was detected using colony formation assay (c1), and the colony number was counted (c2). Gtf3a mRNA expression, cell colony number, and cell viability are expressed as the mean ± SEM of three independent experiments. a P

    Article Snippet: Human CRC cell lines (HCT116, SW480, DLD1, SW620, and HT29) were obtained from the American Type Culture Collection (Manassas, VA, United States) and were purchased from the Shanghai Cell Center (Shanghai, China).

    Techniques: Expressing, Western Blot, Stable Transfection, Transfection, Real-time Polymerase Chain Reaction, Cell Counting, Colony Assay

    Knockdown of transcriptional factor III A gene inhibits the invasion and migration of colorectal cancer cell in vitro . A: The migratory abilities of short hairpin (sh) GTF3A#1 and #4-HCT116 cells were detected using wound-healing assay (a1). The migratory abilities of shGTF3A#1 and #4-SW480 cells were detected as above (a2); B: The migratory and invasive capabilities of shGTF3A#1 and #4-HCT116 (b1) and shGTF3A#1 and #4-SW480 cells (b2) were detected using transwell assay. The migrated and invaded cells were counted (b3). Migratory and invasive capabilities are expressed as the mean ± SEM of three independent experiments. c P

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: Transcriptional factor III A promotes colorectal cancer progression by upregulating cystatin A

    doi: 10.4251/wjgo.v14.i10.1918

    Figure Lengend Snippet: Knockdown of transcriptional factor III A gene inhibits the invasion and migration of colorectal cancer cell in vitro . A: The migratory abilities of short hairpin (sh) GTF3A#1 and #4-HCT116 cells were detected using wound-healing assay (a1). The migratory abilities of shGTF3A#1 and #4-SW480 cells were detected as above (a2); B: The migratory and invasive capabilities of shGTF3A#1 and #4-HCT116 (b1) and shGTF3A#1 and #4-SW480 cells (b2) were detected using transwell assay. The migrated and invaded cells were counted (b3). Migratory and invasive capabilities are expressed as the mean ± SEM of three independent experiments. c P

    Article Snippet: Human CRC cell lines (HCT116, SW480, DLD1, SW620, and HT29) were obtained from the American Type Culture Collection (Manassas, VA, United States) and were purchased from the Shanghai Cell Center (Shanghai, China).

    Techniques: Migration, In Vitro, Wound Healing Assay, Transwell Assay

    Transcriptional factor III A regulates cystatin A by binding to the promoter of cystatin A gene. A: Heat map of RNA-sequencing (RNA-Seq) for transcriptional factor III A gene (Gtf3a)- knockdown and scramble control cells; B: Volcano plot of RNA-Seq for Gtf3a- knockdown and scramble control cells; C: mRNA expression of Gtf3a , cystatin A ( Csta) , cystatin SN gene ( Cst1 ), and cystatin S genes ( Cst4 ) in short hairpin (sh)scramble-SW480 and shGTF3A#1 and #4-SW480 cells were detected using real-time quantitative polymerase chain reaction; D: GTF3A, CSTA, CST1, and CST4 in shscramble-SW480 and shGTF3A#1 and #4-SW480 cells were detected using Western blot; E: RNA fluorescence in situ hybridization was performed to verify the locations of the Csta promoter probe (lncRNA) and GTF3A in SW480 cells; F: Electrophoretic mobility shift assay (EMSA) was used to test the interaction of the Csta promoter and GTF3A. The Csta promoter plus GTF3A antibody as the super shift in EMSA; G: Luciferase activity assay was used to detect the interaction of GTF3A with the Csta promoter and the transcription of Csta . Group 1 ( Csta promoter-luc blank vector plus GTF3A blank plasmid) and group 2 ( Csta promoter-luc blank vector plus GTF3A-plasmid) served as the control groups, and group 3 ( Csta promoter-luc plus GTF3A) and group 4 ( Csta promoter-luc plus GTF3A blank vector) as experimental groups. Csta expression is expressed as the mean ± SEM of three independent experiments. c P

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: Transcriptional factor III A promotes colorectal cancer progression by upregulating cystatin A

    doi: 10.4251/wjgo.v14.i10.1918

    Figure Lengend Snippet: Transcriptional factor III A regulates cystatin A by binding to the promoter of cystatin A gene. A: Heat map of RNA-sequencing (RNA-Seq) for transcriptional factor III A gene (Gtf3a)- knockdown and scramble control cells; B: Volcano plot of RNA-Seq for Gtf3a- knockdown and scramble control cells; C: mRNA expression of Gtf3a , cystatin A ( Csta) , cystatin SN gene ( Cst1 ), and cystatin S genes ( Cst4 ) in short hairpin (sh)scramble-SW480 and shGTF3A#1 and #4-SW480 cells were detected using real-time quantitative polymerase chain reaction; D: GTF3A, CSTA, CST1, and CST4 in shscramble-SW480 and shGTF3A#1 and #4-SW480 cells were detected using Western blot; E: RNA fluorescence in situ hybridization was performed to verify the locations of the Csta promoter probe (lncRNA) and GTF3A in SW480 cells; F: Electrophoretic mobility shift assay (EMSA) was used to test the interaction of the Csta promoter and GTF3A. The Csta promoter plus GTF3A antibody as the super shift in EMSA; G: Luciferase activity assay was used to detect the interaction of GTF3A with the Csta promoter and the transcription of Csta . Group 1 ( Csta promoter-luc blank vector plus GTF3A blank plasmid) and group 2 ( Csta promoter-luc blank vector plus GTF3A-plasmid) served as the control groups, and group 3 ( Csta promoter-luc plus GTF3A) and group 4 ( Csta promoter-luc plus GTF3A blank vector) as experimental groups. Csta expression is expressed as the mean ± SEM of three independent experiments. c P

    Article Snippet: Human CRC cell lines (HCT116, SW480, DLD1, SW620, and HT29) were obtained from the American Type Culture Collection (Manassas, VA, United States) and were purchased from the Shanghai Cell Center (Shanghai, China).

    Techniques: Binding Assay, RNA Sequencing Assay, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Fluorescence, In Situ Hybridization, Electrophoretic Mobility Shift Assay, Luciferase, Activity Assay, Plasmid Preparation

    Transcriptional factor III A promotes colorectal cancer growth in vivo . A: Short hairpin of transcriptional factor III A (shGTF3A)-HCT116 and short hairpin of scramble (shscramble)-HCT116 cells were subcutaneously injected into the right armpit of nude mice. After 28 d, the mice were euthanized, and the images of the representative nude mice are shown; B: Tumors were stripped from the nude mouse; C: The tumor growth curve of shGTF3A-HCT116 and shscramble-HCT116 cells was calculated by tumor volume; D: The removed tumors of shGTF3A-HCT116 and shscramble-HCT116 cells were weighed; E: Schematic diagram of GTF3A-promoting CRC metastasis. GTF3A bound to the promoter of cystatin A ( Csta ) gene to increase Csta gene transcription and protein expression, increased CSTA regulated the epithelial-mesenchymal transition (EMT) to promote invasion and metastasis of colorectal cancer (CRC) cells, while knockdown of Gtf3a decreased CSTA expression, inhibited the EMT, and reduced CRC cell invasion and metastasis. a P

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: Transcriptional factor III A promotes colorectal cancer progression by upregulating cystatin A

    doi: 10.4251/wjgo.v14.i10.1918

    Figure Lengend Snippet: Transcriptional factor III A promotes colorectal cancer growth in vivo . A: Short hairpin of transcriptional factor III A (shGTF3A)-HCT116 and short hairpin of scramble (shscramble)-HCT116 cells were subcutaneously injected into the right armpit of nude mice. After 28 d, the mice were euthanized, and the images of the representative nude mice are shown; B: Tumors were stripped from the nude mouse; C: The tumor growth curve of shGTF3A-HCT116 and shscramble-HCT116 cells was calculated by tumor volume; D: The removed tumors of shGTF3A-HCT116 and shscramble-HCT116 cells were weighed; E: Schematic diagram of GTF3A-promoting CRC metastasis. GTF3A bound to the promoter of cystatin A ( Csta ) gene to increase Csta gene transcription and protein expression, increased CSTA regulated the epithelial-mesenchymal transition (EMT) to promote invasion and metastasis of colorectal cancer (CRC) cells, while knockdown of Gtf3a decreased CSTA expression, inhibited the EMT, and reduced CRC cell invasion and metastasis. a P

    Article Snippet: Human CRC cell lines (HCT116, SW480, DLD1, SW620, and HT29) were obtained from the American Type Culture Collection (Manassas, VA, United States) and were purchased from the Shanghai Cell Center (Shanghai, China).

    Techniques: In Vivo, Injection, Mouse Assay, Expressing

    Transcriptional factor III A expression in colorectal cancer and survival analysis of patients with colorectal cancer. A: Transcriptional factor III A (GTF3A) expression in adjacent normal, colorectal cancer (CRC), and metastatic tissues were detected using immunohistochemical staining. The grading standards were: (1) Negative, a, scored as 0; (2) Weakly positive, b, scored as 1; (3) Moderately positive, c, scored as 2; and (4) Strongly positive, d, scored as 3. Scale bar, 50 μm; B: GTF3A expression in adjacent normal, CRC, and metastatic tissues was quantified using semi-quantitative histological score. Scored dots expression groups were statistically analyzed using unpaired t test; C: Overall survival of patients with GTF3A negative ( n = 25) or GTF3A positive ( n = 56) expression was analyzed by log-rank (Mantel-Cox) test. b P

    Journal: World Journal of Gastrointestinal Oncology

    Article Title: Transcriptional factor III A promotes colorectal cancer progression by upregulating cystatin A

    doi: 10.4251/wjgo.v14.i10.1918

    Figure Lengend Snippet: Transcriptional factor III A expression in colorectal cancer and survival analysis of patients with colorectal cancer. A: Transcriptional factor III A (GTF3A) expression in adjacent normal, colorectal cancer (CRC), and metastatic tissues were detected using immunohistochemical staining. The grading standards were: (1) Negative, a, scored as 0; (2) Weakly positive, b, scored as 1; (3) Moderately positive, c, scored as 2; and (4) Strongly positive, d, scored as 3. Scale bar, 50 μm; B: GTF3A expression in adjacent normal, CRC, and metastatic tissues was quantified using semi-quantitative histological score. Scored dots expression groups were statistically analyzed using unpaired t test; C: Overall survival of patients with GTF3A negative ( n = 25) or GTF3A positive ( n = 56) expression was analyzed by log-rank (Mantel-Cox) test. b P

    Article Snippet: Human CRC cell lines (HCT116, SW480, DLD1, SW620, and HT29) were obtained from the American Type Culture Collection (Manassas, VA, United States) and were purchased from the Shanghai Cell Center (Shanghai, China).

    Techniques: Expressing, Immunohistochemistry, Staining

    SUCNR1 promotes the migration and invasion of CRC cells by blunting tumor cell autophagy. (a) SUCNR1 mRNA expression in HCT-116 cells treated with sh-SUCNR1 determined by RT-qPCR. (b) Viability of HCT-116 cells following SUCNR1 knockdown or combined with 3-MA measured by CCK-8 assay. (c) Migration of HCT-116 cells following SUCNR1 knockdown or combined with 3-MA measured by Transwell assay. (d) Invasion of HCT-116 cells following SUCNR1 knockdown or combined with 3-MA measured by Transwell assay. (e) Flow cytometric analysis of the HCT-116 cell apoptosis following SUCNR1 knockdown or combined with 3-MA. (f) Western blot analysis of LC3-II/LC3-I ratio in HCT-116 cells following SUCNR1 knockdown or combined with 3-MA. (g) Immunofluorescence detection of the number of GFP-LC3 spots in HCT-116 cells following SUCNR1 knockdown or combined with 3-MA (scale bar = 50 μ m). (h) Number of autophagic vacuoles in HCT-116 cells following SUCNR1 knockdown or combined with 3-MA under a TEM. ∗ p

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: HDAC8 Promotes Liver Metastasis of Colorectal Cancer via Inhibition of IRF1 and Upregulation of SUCNR1

    doi: 10.1155/2022/2815187

    Figure Lengend Snippet: SUCNR1 promotes the migration and invasion of CRC cells by blunting tumor cell autophagy. (a) SUCNR1 mRNA expression in HCT-116 cells treated with sh-SUCNR1 determined by RT-qPCR. (b) Viability of HCT-116 cells following SUCNR1 knockdown or combined with 3-MA measured by CCK-8 assay. (c) Migration of HCT-116 cells following SUCNR1 knockdown or combined with 3-MA measured by Transwell assay. (d) Invasion of HCT-116 cells following SUCNR1 knockdown or combined with 3-MA measured by Transwell assay. (e) Flow cytometric analysis of the HCT-116 cell apoptosis following SUCNR1 knockdown or combined with 3-MA. (f) Western blot analysis of LC3-II/LC3-I ratio in HCT-116 cells following SUCNR1 knockdown or combined with 3-MA. (g) Immunofluorescence detection of the number of GFP-LC3 spots in HCT-116 cells following SUCNR1 knockdown or combined with 3-MA (scale bar = 50 μ m). (h) Number of autophagic vacuoles in HCT-116 cells following SUCNR1 knockdown or combined with 3-MA under a TEM. ∗ p

    Article Snippet: Four human CRC cell lines (namely, SW480, SW620, HT29, and HCT-116), human normal colorectal epithelial cell line FHC, and HEK293T cells (all procured from American Type Culture Collection, Manassas, VA) were cultured in Dulbecco's modified Eagle's medium (10569044, Gibco, Grand Island, NY) appended to 10% fetal bovine serum (FBS; 10099141, Gibco), 2 mM L-glutamine (Sigma-Aldrich, St Louis, MO), 100 U/mL penicillin, and 100 μ g/mL streptomycin in a 5% CO2 incubator at 37°C.

    Techniques: Migration, Expressing, Quantitative RT-PCR, CCK-8 Assay, Transwell Assay, Western Blot, Immunofluorescence, Transmission Electron Microscopy

    HDAC8 suppresses cell autophagy to boost the migration and invasion of CRC cells by regulating the IRF1/SUCNR1 axis. HCT-116 cells were transfected with sh-HDAC8 or combined with oe-SUCNR1. (a) SUCNR1 mRNA expression in HCT-116 cells determined by RT-qPCR. (b) Viability of HCT-116 cells measured by CCK-8 assay. (c) Migration of HCT-116 cells measured by Transwell assay. (d) Invasion of HCT-116 cells measured by Transwell assay. (e) Western blot analysis of LC3-II/LC3-I ratio in HCT-116 cells. (f) Immunofluorescence detection of the number of GFP-LC3 spots in HCT-116 cells (scale bar = 50 μ m). (g) Number of autophagic vacuoles in HCT-116 cells under a TEM. ∗ p

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: HDAC8 Promotes Liver Metastasis of Colorectal Cancer via Inhibition of IRF1 and Upregulation of SUCNR1

    doi: 10.1155/2022/2815187

    Figure Lengend Snippet: HDAC8 suppresses cell autophagy to boost the migration and invasion of CRC cells by regulating the IRF1/SUCNR1 axis. HCT-116 cells were transfected with sh-HDAC8 or combined with oe-SUCNR1. (a) SUCNR1 mRNA expression in HCT-116 cells determined by RT-qPCR. (b) Viability of HCT-116 cells measured by CCK-8 assay. (c) Migration of HCT-116 cells measured by Transwell assay. (d) Invasion of HCT-116 cells measured by Transwell assay. (e) Western blot analysis of LC3-II/LC3-I ratio in HCT-116 cells. (f) Immunofluorescence detection of the number of GFP-LC3 spots in HCT-116 cells (scale bar = 50 μ m). (g) Number of autophagic vacuoles in HCT-116 cells under a TEM. ∗ p

    Article Snippet: Four human CRC cell lines (namely, SW480, SW620, HT29, and HCT-116), human normal colorectal epithelial cell line FHC, and HEK293T cells (all procured from American Type Culture Collection, Manassas, VA) were cultured in Dulbecco's modified Eagle's medium (10569044, Gibco, Grand Island, NY) appended to 10% fetal bovine serum (FBS; 10099141, Gibco), 2 mM L-glutamine (Sigma-Aldrich, St Louis, MO), 100 U/mL penicillin, and 100 μ g/mL streptomycin in a 5% CO2 incubator at 37°C.

    Techniques: Migration, Transfection, Expressing, Quantitative RT-PCR, CCK-8 Assay, Transwell Assay, Western Blot, Immunofluorescence, Transmission Electron Microscopy

    HDAC8 suppresses the expression of IRF1 and thus facilitates the growth and metastasis of CRC cells. (a) HDAC8 and IRF1 mRNA expression in CRC and adjacent normal tissues determined by RT-qPCR ( n = 58). (b) HDAC8 and IRF1 mRNA expression in SW480, SW620, HT29, HCT-116, and FHC cell lines determined by RT-qPCR. (c) Histone acetylation levels in the IRF1 promoter region in CRC and adjacent normal tissues determined by ChIP. (d) mRNA expression of HDAC8 and IRF1 in HCT-116 cells treated with sh-HDAC8 or oe-HDAC8 determined by RT-qPCR. (e) Western blot analysis of HDAC8 and IRF1 proteins in HCT-116 cells treated with sh-HDAC8 or oe-HDAC8. (f) mRNA expression of HDAC8 and IRF1 in HCT-116 cells treated with PCI-34051 determined by RT-qPCR. (g) H3K9Ac levels in the IRF1 promoter region in HCT-116 cells treated with PCI-34051 determined by ChIP. (h) HDAC8 and IRF1 mRNA expression in HCT-116 cells treated with sh-HDAC8 or combined with sh-IRF1 determined by RT-qPCR. (i) Viability of HCT-116 cells treated with sh-HDAC8 or combined with sh-IRF1 measured by CCK-8 assay. (j) Migration of HCT-116 cells treated with sh-HDAC8 or combined with sh-IRF1 measured by Transwell assay. (k) Invasion of HCT-116 cells treated with sh-HDAC8 or combined with sh-IRF1 measured by Transwell assay. ∗ p

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: HDAC8 Promotes Liver Metastasis of Colorectal Cancer via Inhibition of IRF1 and Upregulation of SUCNR1

    doi: 10.1155/2022/2815187

    Figure Lengend Snippet: HDAC8 suppresses the expression of IRF1 and thus facilitates the growth and metastasis of CRC cells. (a) HDAC8 and IRF1 mRNA expression in CRC and adjacent normal tissues determined by RT-qPCR ( n = 58). (b) HDAC8 and IRF1 mRNA expression in SW480, SW620, HT29, HCT-116, and FHC cell lines determined by RT-qPCR. (c) Histone acetylation levels in the IRF1 promoter region in CRC and adjacent normal tissues determined by ChIP. (d) mRNA expression of HDAC8 and IRF1 in HCT-116 cells treated with sh-HDAC8 or oe-HDAC8 determined by RT-qPCR. (e) Western blot analysis of HDAC8 and IRF1 proteins in HCT-116 cells treated with sh-HDAC8 or oe-HDAC8. (f) mRNA expression of HDAC8 and IRF1 in HCT-116 cells treated with PCI-34051 determined by RT-qPCR. (g) H3K9Ac levels in the IRF1 promoter region in HCT-116 cells treated with PCI-34051 determined by ChIP. (h) HDAC8 and IRF1 mRNA expression in HCT-116 cells treated with sh-HDAC8 or combined with sh-IRF1 determined by RT-qPCR. (i) Viability of HCT-116 cells treated with sh-HDAC8 or combined with sh-IRF1 measured by CCK-8 assay. (j) Migration of HCT-116 cells treated with sh-HDAC8 or combined with sh-IRF1 measured by Transwell assay. (k) Invasion of HCT-116 cells treated with sh-HDAC8 or combined with sh-IRF1 measured by Transwell assay. ∗ p

    Article Snippet: Four human CRC cell lines (namely, SW480, SW620, HT29, and HCT-116), human normal colorectal epithelial cell line FHC, and HEK293T cells (all procured from American Type Culture Collection, Manassas, VA) were cultured in Dulbecco's modified Eagle's medium (10569044, Gibco, Grand Island, NY) appended to 10% fetal bovine serum (FBS; 10099141, Gibco), 2 mM L-glutamine (Sigma-Aldrich, St Louis, MO), 100 U/mL penicillin, and 100 μ g/mL streptomycin in a 5% CO2 incubator at 37°C.

    Techniques: Expressing, Quantitative RT-PCR, Chromatin Immunoprecipitation, Western Blot, CCK-8 Assay, Migration, Transwell Assay

    Molecular mechanism by which HDAC8 regulates the progression of CRC. Histone deacetylase HDAC8 upregulates SUCNR1 by downregulating IRF1 and consequently inhibits CRC cell autophagy, ultimately contributing to the CRC growth and liver metastasis.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: HDAC8 Promotes Liver Metastasis of Colorectal Cancer via Inhibition of IRF1 and Upregulation of SUCNR1

    doi: 10.1155/2022/2815187

    Figure Lengend Snippet: Molecular mechanism by which HDAC8 regulates the progression of CRC. Histone deacetylase HDAC8 upregulates SUCNR1 by downregulating IRF1 and consequently inhibits CRC cell autophagy, ultimately contributing to the CRC growth and liver metastasis.

    Article Snippet: Four human CRC cell lines (namely, SW480, SW620, HT29, and HCT-116), human normal colorectal epithelial cell line FHC, and HEK293T cells (all procured from American Type Culture Collection, Manassas, VA) were cultured in Dulbecco's modified Eagle's medium (10569044, Gibco, Grand Island, NY) appended to 10% fetal bovine serum (FBS; 10099141, Gibco), 2 mM L-glutamine (Sigma-Aldrich, St Louis, MO), 100 U/mL penicillin, and 100 μ g/mL streptomycin in a 5% CO2 incubator at 37°C.

    Techniques: Histone Deacetylase Assay

    IRF1 downregulates the expression of SUCNR1 by binding to its promoter in CRC cells. (a) SUCNR1 mRNA expression in CRC and adjacent normal tissues determined by RT-qPCR ( n = 58). (b) SUCNR1 mRNA expression in SW480, SW620, HT29, HCT-116, and FHC cell lines determined by RT-qPCR. (c) Prediction of IRF1 binding sites in the SUCNR1 promoter and mutation sequence generated by site mutation determined by ChIP. (d) Binding between IRF1 and SUCNR1 confirmed by dual-luciferase reporter assay. (e) Enrichment of IRF1 in the promoter of SUCNR1 determined by ChIP. (f) IRF1 and SUCNR1 mRNA expression in HCT-116 cells treated with sh-IRF1 or oe-IRF1 determined by RT-qPCR. (g) Western blot analysis of IRF1 and SUCNR1 proteins in HCT-116 cells treated with sh-IRF1 or oe-IRF1. ∗∗ p

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: HDAC8 Promotes Liver Metastasis of Colorectal Cancer via Inhibition of IRF1 and Upregulation of SUCNR1

    doi: 10.1155/2022/2815187

    Figure Lengend Snippet: IRF1 downregulates the expression of SUCNR1 by binding to its promoter in CRC cells. (a) SUCNR1 mRNA expression in CRC and adjacent normal tissues determined by RT-qPCR ( n = 58). (b) SUCNR1 mRNA expression in SW480, SW620, HT29, HCT-116, and FHC cell lines determined by RT-qPCR. (c) Prediction of IRF1 binding sites in the SUCNR1 promoter and mutation sequence generated by site mutation determined by ChIP. (d) Binding between IRF1 and SUCNR1 confirmed by dual-luciferase reporter assay. (e) Enrichment of IRF1 in the promoter of SUCNR1 determined by ChIP. (f) IRF1 and SUCNR1 mRNA expression in HCT-116 cells treated with sh-IRF1 or oe-IRF1 determined by RT-qPCR. (g) Western blot analysis of IRF1 and SUCNR1 proteins in HCT-116 cells treated with sh-IRF1 or oe-IRF1. ∗∗ p

    Article Snippet: Four human CRC cell lines (namely, SW480, SW620, HT29, and HCT-116), human normal colorectal epithelial cell line FHC, and HEK293T cells (all procured from American Type Culture Collection, Manassas, VA) were cultured in Dulbecco's modified Eagle's medium (10569044, Gibco, Grand Island, NY) appended to 10% fetal bovine serum (FBS; 10099141, Gibco), 2 mM L-glutamine (Sigma-Aldrich, St Louis, MO), 100 U/mL penicillin, and 100 μ g/mL streptomycin in a 5% CO2 incubator at 37°C.

    Techniques: Expressing, Binding Assay, Quantitative RT-PCR, Mutagenesis, Sequencing, Generated, Chromatin Immunoprecipitation, Luciferase, Reporter Assay, Western Blot

    Significance of the HDAC8/IRF1/SUCNR1 axis in CRC. (a) A box plot of the differential expression of HDAC8 in the colon adenocarcinoma (COAD) and rectum adenocarcinoma (READ) samples included in TCGA and GTEx (red box plots represent tumor samples, and gray box plots represent normal samples; in COAD, there are 275 tumor samples and 349 normal samples; in READ, there are 92 tumor samples and 318 normal samples). (b) Venn diagram of HDAC8 downstream regulatory genes and transcription factors (the left is the downstream genes of HDAC8 predicted by the starBase database, the right is the transcription factor annotation, and the center represents the intersection of the two sets of data). (c) Interaction analysis of the candidate transcription factors; each circle in the figure represents a gene, and the line between circles indicates interaction between two genes; the darker color of the circle where the gene is located reflects more interaction genes, higher core degree in the interaction network, and higher degree value. (d) Statistics of degree value of core genes in the gene interaction network (the abscissa represents the degree value and the ordinate represents the gene name). (e) KEGG enrichment analysis of the candidate transcription factors (the abscissa represents the gene ratio, the ordinate represents the KEGG entry identifier, and the histogram on the right is the color scale). (f) A box plot of the differential expression of SUCNR1 in the CRC included in TCGA and GTEx (red box plots represent tumor samples, and gray box plots represent normal samples; in COAD, there are 275 tumor samples and 349 normal samples; in READ, there are 92 tumor samples and 318 normal samples). ∗ p

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: HDAC8 Promotes Liver Metastasis of Colorectal Cancer via Inhibition of IRF1 and Upregulation of SUCNR1

    doi: 10.1155/2022/2815187

    Figure Lengend Snippet: Significance of the HDAC8/IRF1/SUCNR1 axis in CRC. (a) A box plot of the differential expression of HDAC8 in the colon adenocarcinoma (COAD) and rectum adenocarcinoma (READ) samples included in TCGA and GTEx (red box plots represent tumor samples, and gray box plots represent normal samples; in COAD, there are 275 tumor samples and 349 normal samples; in READ, there are 92 tumor samples and 318 normal samples). (b) Venn diagram of HDAC8 downstream regulatory genes and transcription factors (the left is the downstream genes of HDAC8 predicted by the starBase database, the right is the transcription factor annotation, and the center represents the intersection of the two sets of data). (c) Interaction analysis of the candidate transcription factors; each circle in the figure represents a gene, and the line between circles indicates interaction between two genes; the darker color of the circle where the gene is located reflects more interaction genes, higher core degree in the interaction network, and higher degree value. (d) Statistics of degree value of core genes in the gene interaction network (the abscissa represents the degree value and the ordinate represents the gene name). (e) KEGG enrichment analysis of the candidate transcription factors (the abscissa represents the gene ratio, the ordinate represents the KEGG entry identifier, and the histogram on the right is the color scale). (f) A box plot of the differential expression of SUCNR1 in the CRC included in TCGA and GTEx (red box plots represent tumor samples, and gray box plots represent normal samples; in COAD, there are 275 tumor samples and 349 normal samples; in READ, there are 92 tumor samples and 318 normal samples). ∗ p

    Article Snippet: Four human CRC cell lines (namely, SW480, SW620, HT29, and HCT-116), human normal colorectal epithelial cell line FHC, and HEK293T cells (all procured from American Type Culture Collection, Manassas, VA) were cultured in Dulbecco's modified Eagle's medium (10569044, Gibco, Grand Island, NY) appended to 10% fetal bovine serum (FBS; 10099141, Gibco), 2 mM L-glutamine (Sigma-Aldrich, St Louis, MO), 100 U/mL penicillin, and 100 μ g/mL streptomycin in a 5% CO2 incubator at 37°C.

    Techniques: Expressing

    HDAC8 promotes tumorigenesis and liver metastasis of CRC cells by regulating the IRF1/SUCNR1 axis in nude mice. (a) Tumor growth of mice treated with sh-HDAC8 or combined with oe-SUCNR1. (b) Ki67 immunohistochemical staining images of tumor tissues of nude mice treated with sh-HDAC8 or combined with oe-SUCNR1 as well as the semiquantitative analysis. (c) mRNA expression of HDAC8, IRF1, and SUCNR1 in tumor tissues of mice treated with sh-HDAC8 or combined with oe-SUCNR1 determined by RT-qPCR. (d) HE staining analysis of number of liver metastases in the liver tissues of nude mice treated with sh-HDAC8 or combined with oe-SUCNR1 (scale bar = 50 μ m). n = 10 for mice upon each treatment. ∗ p

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: HDAC8 Promotes Liver Metastasis of Colorectal Cancer via Inhibition of IRF1 and Upregulation of SUCNR1

    doi: 10.1155/2022/2815187

    Figure Lengend Snippet: HDAC8 promotes tumorigenesis and liver metastasis of CRC cells by regulating the IRF1/SUCNR1 axis in nude mice. (a) Tumor growth of mice treated with sh-HDAC8 or combined with oe-SUCNR1. (b) Ki67 immunohistochemical staining images of tumor tissues of nude mice treated with sh-HDAC8 or combined with oe-SUCNR1 as well as the semiquantitative analysis. (c) mRNA expression of HDAC8, IRF1, and SUCNR1 in tumor tissues of mice treated with sh-HDAC8 or combined with oe-SUCNR1 determined by RT-qPCR. (d) HE staining analysis of number of liver metastases in the liver tissues of nude mice treated with sh-HDAC8 or combined with oe-SUCNR1 (scale bar = 50 μ m). n = 10 for mice upon each treatment. ∗ p

    Article Snippet: Four human CRC cell lines (namely, SW480, SW620, HT29, and HCT-116), human normal colorectal epithelial cell line FHC, and HEK293T cells (all procured from American Type Culture Collection, Manassas, VA) were cultured in Dulbecco's modified Eagle's medium (10569044, Gibco, Grand Island, NY) appended to 10% fetal bovine serum (FBS; 10099141, Gibco), 2 mM L-glutamine (Sigma-Aldrich, St Louis, MO), 100 U/mL penicillin, and 100 μ g/mL streptomycin in a 5% CO2 incubator at 37°C.

    Techniques: Mouse Assay, Immunohistochemistry, Staining, Expressing, Quantitative RT-PCR

    MiR-663b can reverse the inhibitive effects of circ_0003215 in CRC cells. A Correlation analysis between the expression levels of circ_0003215 and miR-663b expression. B FISH analysis of circ_0003215(red) and miR-663b(green) in HT29 cells transfected with empty vector or circ_0003215 plasmid. C , D CCK8 and EdU analysis of the proliferation capacities in HT29 or SW480 cells with diferent transfection. E Colony formation assay of HT29 or SW480 cells transfected with diferent transfection F Wound healing assay to evaluate the cell migration of HT29 cells with diferent transfection. G , H Transwell assay for the invasion and migration ability of CRC cells transfected with indicated vectors. Graph represents mean ± SD; * P

    Journal: Cell Death & Disease

    Article Title: N6-methyladenosine modification of circ_0003215 suppresses the pentose phosphate pathway and malignancy of colorectal cancer through the miR-663b/DLG4/G6PD axis

    doi: 10.1038/s41419-022-05245-2

    Figure Lengend Snippet: MiR-663b can reverse the inhibitive effects of circ_0003215 in CRC cells. A Correlation analysis between the expression levels of circ_0003215 and miR-663b expression. B FISH analysis of circ_0003215(red) and miR-663b(green) in HT29 cells transfected with empty vector or circ_0003215 plasmid. C , D CCK8 and EdU analysis of the proliferation capacities in HT29 or SW480 cells with diferent transfection. E Colony formation assay of HT29 or SW480 cells transfected with diferent transfection F Wound healing assay to evaluate the cell migration of HT29 cells with diferent transfection. G , H Transwell assay for the invasion and migration ability of CRC cells transfected with indicated vectors. Graph represents mean ± SD; * P

    Article Snippet: The CRC cell lines (SW620, HCT116, SW480, DLD-1, LOVO, and HT29) and the human embryonic kidney epithelial cell line (HEK-293T) were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Expressing, Fluorescence In Situ Hybridization, Transfection, Plasmid Preparation, Colony Assay, Wound Healing Assay, Migration, Transwell Assay

    DLG4 regulates PPP through the K48-linked ubiquitination of G6PD. A GSEA analysis showed that low DLG4 expression associated with pentose phosphate pathway, ubiquitin-mediated proteolysis, DNA replication and oxidative phosphorylation. B The mRNA levels of DLG4, G6PD, 6PGL and 6PGD were detected in SW480 cells using RT-qPCR, upon overexpression or knockdown of DLG4. C The expression of DLG4, G6PD, 6PGL and 6PGD proteins levels were analyzed following DLG4 knockdown and DLG4 overexpression in CRC cells. D Degradation of G6PD was investigated using western blot analysis in a CHX chase assay in SW480 cells after DLG4 overexpression or knockdown. E The immunoprecipitation / western blotting assays were used to detect the ubiquitination levels of G6PD protein in SW480 cells after overexpression or knockdown of DLG4. F DLG4 induced K48-linked ubiquitination of G6PD in HEK-293T cells. G Illustration of the mechanism of circ_0003215 on promoting CRC pathogenesis and metastasis via miR-663b/DLG4/G6PD axis-mediated pentose phosphate pathway.

    Journal: Cell Death & Disease

    Article Title: N6-methyladenosine modification of circ_0003215 suppresses the pentose phosphate pathway and malignancy of colorectal cancer through the miR-663b/DLG4/G6PD axis

    doi: 10.1038/s41419-022-05245-2

    Figure Lengend Snippet: DLG4 regulates PPP through the K48-linked ubiquitination of G6PD. A GSEA analysis showed that low DLG4 expression associated with pentose phosphate pathway, ubiquitin-mediated proteolysis, DNA replication and oxidative phosphorylation. B The mRNA levels of DLG4, G6PD, 6PGL and 6PGD were detected in SW480 cells using RT-qPCR, upon overexpression or knockdown of DLG4. C The expression of DLG4, G6PD, 6PGL and 6PGD proteins levels were analyzed following DLG4 knockdown and DLG4 overexpression in CRC cells. D Degradation of G6PD was investigated using western blot analysis in a CHX chase assay in SW480 cells after DLG4 overexpression or knockdown. E The immunoprecipitation / western blotting assays were used to detect the ubiquitination levels of G6PD protein in SW480 cells after overexpression or knockdown of DLG4. F DLG4 induced K48-linked ubiquitination of G6PD in HEK-293T cells. G Illustration of the mechanism of circ_0003215 on promoting CRC pathogenesis and metastasis via miR-663b/DLG4/G6PD axis-mediated pentose phosphate pathway.

    Article Snippet: The CRC cell lines (SW620, HCT116, SW480, DLD-1, LOVO, and HT29) and the human embryonic kidney epithelial cell line (HEK-293T) were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Expressing, Quantitative RT-PCR, Over Expression, Western Blot, Immunoprecipitation

    DLG4 is a direct target of circ_0003215/miR-663b axis in CRC cells. A The intersection of the target genes of miR-663b predicted by miRBase, miRWalk, and TargetScan. B The expression of potential miR-663b target genes in SW480 cells transfected with miR-663b mimics or circ_0003215-specific siRNA. C The expression of potential miR-663b target genes in HT29 cells transfected with miR-663b mimics or circ_0003215-specific siRNA. D Immunohistochemistry showed the DLG4 protein levels in CRC tissues and normal colorectal mucosa from HPA database. E The expresssion level of DLG4 mRNA in SW480 and HT29 cells transfected with circ_0003215 siRNA or miR-663b inhibitors. F Western blotting of DLG4 was detected in SW480 cells after transfecting with indicated vectors. G Three-dimensional scatter plot of circ_0003215, miR-663b and DLG4 in 50 paired CRC and adjacent tissues. H Schematic representation of the DLG4 3’-UTR WT and DLG4 3’-UTR MUT luciferase reporter vectors(left). The relative luciferase activity in HEK-293T co-transfected with miR-663b mimics or NC and the DLG4 3’-UTR WT or MUT reporter vectors (right). * P

    Journal: Cell Death & Disease

    Article Title: N6-methyladenosine modification of circ_0003215 suppresses the pentose phosphate pathway and malignancy of colorectal cancer through the miR-663b/DLG4/G6PD axis

    doi: 10.1038/s41419-022-05245-2

    Figure Lengend Snippet: DLG4 is a direct target of circ_0003215/miR-663b axis in CRC cells. A The intersection of the target genes of miR-663b predicted by miRBase, miRWalk, and TargetScan. B The expression of potential miR-663b target genes in SW480 cells transfected with miR-663b mimics or circ_0003215-specific siRNA. C The expression of potential miR-663b target genes in HT29 cells transfected with miR-663b mimics or circ_0003215-specific siRNA. D Immunohistochemistry showed the DLG4 protein levels in CRC tissues and normal colorectal mucosa from HPA database. E The expresssion level of DLG4 mRNA in SW480 and HT29 cells transfected with circ_0003215 siRNA or miR-663b inhibitors. F Western blotting of DLG4 was detected in SW480 cells after transfecting with indicated vectors. G Three-dimensional scatter plot of circ_0003215, miR-663b and DLG4 in 50 paired CRC and adjacent tissues. H Schematic representation of the DLG4 3’-UTR WT and DLG4 3’-UTR MUT luciferase reporter vectors(left). The relative luciferase activity in HEK-293T co-transfected with miR-663b mimics or NC and the DLG4 3’-UTR WT or MUT reporter vectors (right). * P

    Article Snippet: The CRC cell lines (SW620, HCT116, SW480, DLD-1, LOVO, and HT29) and the human embryonic kidney epithelial cell line (HEK-293T) were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Expressing, Transfection, Immunohistochemistry, Western Blot, Luciferase, Activity Assay

    Circ_0003215 inhibits the tumor growth and metastasis of CRC in vitro. A Schematic flowchart of the subcutaneous tumor formation assay (left). Images of the dissected subcutaneous tumors from the tumor-bearing mice at the end of experiment (right). B Growth curves of xenograft tumors measured every 3 days ( n = 5/group). C The final weight of the xenograft tumor was shown in the the scatter plot. D HE staining of the subcutaneous tumors (×100, ×400). E Expression of DLG4 and Ki67 in subcutaneous tumors assessed by IHC. F RT-qPCR analysis of relative expression of circ_0003215 and miR-663b in subcutaneous tumors. G Measurement of lung weight in the tail vein-lung colonization model (left). Analysis of the lung metastatic nodules under the microscope (right). H Schematic representation of the metastasis assay model (left). Representative images from the lungs and metastatic nodules (right). * P

    Journal: Cell Death & Disease

    Article Title: N6-methyladenosine modification of circ_0003215 suppresses the pentose phosphate pathway and malignancy of colorectal cancer through the miR-663b/DLG4/G6PD axis

    doi: 10.1038/s41419-022-05245-2

    Figure Lengend Snippet: Circ_0003215 inhibits the tumor growth and metastasis of CRC in vitro. A Schematic flowchart of the subcutaneous tumor formation assay (left). Images of the dissected subcutaneous tumors from the tumor-bearing mice at the end of experiment (right). B Growth curves of xenograft tumors measured every 3 days ( n = 5/group). C The final weight of the xenograft tumor was shown in the the scatter plot. D HE staining of the subcutaneous tumors (×100, ×400). E Expression of DLG4 and Ki67 in subcutaneous tumors assessed by IHC. F RT-qPCR analysis of relative expression of circ_0003215 and miR-663b in subcutaneous tumors. G Measurement of lung weight in the tail vein-lung colonization model (left). Analysis of the lung metastatic nodules under the microscope (right). H Schematic representation of the metastasis assay model (left). Representative images from the lungs and metastatic nodules (right). * P

    Article Snippet: The CRC cell lines (SW620, HCT116, SW480, DLD-1, LOVO, and HT29) and the human embryonic kidney epithelial cell line (HEK-293T) were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: In Vitro, Tube Formation Assay, Mouse Assay, Staining, Expressing, Immunohistochemistry, Quantitative RT-PCR, Microscopy

    Expression profiles of circRNAs in CRC and circ_0003215 are downregulated in CRC. A The differentially expressed circRNAs were analyzed in GSE121895 and GSE142837(Heat map). B , C RT-qPCR analysis of circ_0001955 and circ_0003215 in 50 pairs of CRC tissues and adjacent normal tissues. D Schematic drawing illustrating that circ_0003215 arose from exon 7 and 8 of the MYO9B gene. The back-splicing sites (arrow) of circ_0003215 confirmed by Sanger sequencing. E The product of circ_0003215 and liner mRNA amplified by the convergent or divergent primers in SW480 cells by agarose gel electrophoresis. F Relative expression of circ_0003215 in different CRC cell lines. G RT-qPCR analysis for the expression of MYO9B mRNA and circ_0003215 in CRC cells after treatment of RNase R. H Time-course RT-qPCR analysis of circ_0003215 and its linear counterpart MYO9B in SW480 after actinomycin D (5 µg/mL) treatment. I RT-qPCR analysis of circ_0003215 levels in the nuclear and cytoplasmic fractions of CRC cells. J RNA FISH assay for the localization of circ_0003215 in SW480 and HT29 cells. * P

    Journal: Cell Death & Disease

    Article Title: N6-methyladenosine modification of circ_0003215 suppresses the pentose phosphate pathway and malignancy of colorectal cancer through the miR-663b/DLG4/G6PD axis

    doi: 10.1038/s41419-022-05245-2

    Figure Lengend Snippet: Expression profiles of circRNAs in CRC and circ_0003215 are downregulated in CRC. A The differentially expressed circRNAs were analyzed in GSE121895 and GSE142837(Heat map). B , C RT-qPCR analysis of circ_0001955 and circ_0003215 in 50 pairs of CRC tissues and adjacent normal tissues. D Schematic drawing illustrating that circ_0003215 arose from exon 7 and 8 of the MYO9B gene. The back-splicing sites (arrow) of circ_0003215 confirmed by Sanger sequencing. E The product of circ_0003215 and liner mRNA amplified by the convergent or divergent primers in SW480 cells by agarose gel electrophoresis. F Relative expression of circ_0003215 in different CRC cell lines. G RT-qPCR analysis for the expression of MYO9B mRNA and circ_0003215 in CRC cells after treatment of RNase R. H Time-course RT-qPCR analysis of circ_0003215 and its linear counterpart MYO9B in SW480 after actinomycin D (5 µg/mL) treatment. I RT-qPCR analysis of circ_0003215 levels in the nuclear and cytoplasmic fractions of CRC cells. J RNA FISH assay for the localization of circ_0003215 in SW480 and HT29 cells. * P

    Article Snippet: The CRC cell lines (SW620, HCT116, SW480, DLD-1, LOVO, and HT29) and the human embryonic kidney epithelial cell line (HEK-293T) were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Expressing, Quantitative RT-PCR, Sequencing, Amplification, Agarose Gel Electrophoresis, Fluorescence In Situ Hybridization

    YTHDF2-mediated m6A modification drives the degradation of circ_ 0003215. A , B Predicted m6A site and motif of circ_0003215 from SRAMP. C MeRIP assay indicating that circ_0003215 was highly enriched in m6A precipitated fraction. D Western blot analysis demonstrated that only YTHDF2 protein was pull-downed by circ_ 0003215 probe. E Flow diagram of RIP-qPCR and agarose gel electrophoresis for circ_0003215. F YTHDF2 RIP assay to detect circ_0003215 in CRC cells. G RT-qPCR analysis for the expression of circ_0003215 after YTHDF2 overexpression in CRC cells. H MeRIP assays for m6A-modified circ_0003215 in HT29 (left) and SW480 (right) cells treated with empty vector or YTHDF2 overexpression plasmid.

    Journal: Cell Death & Disease

    Article Title: N6-methyladenosine modification of circ_0003215 suppresses the pentose phosphate pathway and malignancy of colorectal cancer through the miR-663b/DLG4/G6PD axis

    doi: 10.1038/s41419-022-05245-2

    Figure Lengend Snippet: YTHDF2-mediated m6A modification drives the degradation of circ_ 0003215. A , B Predicted m6A site and motif of circ_0003215 from SRAMP. C MeRIP assay indicating that circ_0003215 was highly enriched in m6A precipitated fraction. D Western blot analysis demonstrated that only YTHDF2 protein was pull-downed by circ_ 0003215 probe. E Flow diagram of RIP-qPCR and agarose gel electrophoresis for circ_0003215. F YTHDF2 RIP assay to detect circ_0003215 in CRC cells. G RT-qPCR analysis for the expression of circ_0003215 after YTHDF2 overexpression in CRC cells. H MeRIP assays for m6A-modified circ_0003215 in HT29 (left) and SW480 (right) cells treated with empty vector or YTHDF2 overexpression plasmid.

    Article Snippet: The CRC cell lines (SW620, HCT116, SW480, DLD-1, LOVO, and HT29) and the human embryonic kidney epithelial cell line (HEK-293T) were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Modification, Western Blot, Real-time Polymerase Chain Reaction, Agarose Gel Electrophoresis, Quantitative RT-PCR, Expressing, Over Expression, Plasmid Preparation

    Circ_0003215 serves as an efficient miR-663b sponge in CRC. A Correlation analysis between the expression levels of circ_0003215 and linear MYO9B using Pearsons correlation coefficient. B Circ_0003215 was detected by RIP assay and agarose gel electrophoresis. C The potential target miRNAs of circ_ 0003215 predicted by the circBank tools. D The correlation matrix of circ_ 0003215 and predicated miRNAs levels measured by RT-qPCR in 10 CRC patients. (Red: positive correlation; Blue: negative correlation; circle size and color intensity are proportional to correlation coefficients.) E Whole-cell lysates from CRC cells were incubated with biotin-circ_0003215 or NC probe based on the RNA pull-down flow diagram(left), and the enrichment levels of circ_0003215 and predicated miRNAs were analyzed by RT-qPCR in SW480 cells(right). F The heatmap of miRNA sequencing data of 21 pairs of CRC tissues (GSE89143). G FISH asssay showed the colocalization between circ_0003215 and miR-663b in SW480 and HT29 cells. H The structure and the sequence of circ_0003215-WT or circ_0003215- MUT luciferase plasmid(left). The relative luciferase activities of HEK-293T co-transfected with miR-663b mimics and circ_0003215-WT compared to circ_0003215-MUT (right). * P

    Journal: Cell Death & Disease

    Article Title: N6-methyladenosine modification of circ_0003215 suppresses the pentose phosphate pathway and malignancy of colorectal cancer through the miR-663b/DLG4/G6PD axis

    doi: 10.1038/s41419-022-05245-2

    Figure Lengend Snippet: Circ_0003215 serves as an efficient miR-663b sponge in CRC. A Correlation analysis between the expression levels of circ_0003215 and linear MYO9B using Pearsons correlation coefficient. B Circ_0003215 was detected by RIP assay and agarose gel electrophoresis. C The potential target miRNAs of circ_ 0003215 predicted by the circBank tools. D The correlation matrix of circ_ 0003215 and predicated miRNAs levels measured by RT-qPCR in 10 CRC patients. (Red: positive correlation; Blue: negative correlation; circle size and color intensity are proportional to correlation coefficients.) E Whole-cell lysates from CRC cells were incubated with biotin-circ_0003215 or NC probe based on the RNA pull-down flow diagram(left), and the enrichment levels of circ_0003215 and predicated miRNAs were analyzed by RT-qPCR in SW480 cells(right). F The heatmap of miRNA sequencing data of 21 pairs of CRC tissues (GSE89143). G FISH asssay showed the colocalization between circ_0003215 and miR-663b in SW480 and HT29 cells. H The structure and the sequence of circ_0003215-WT or circ_0003215- MUT luciferase plasmid(left). The relative luciferase activities of HEK-293T co-transfected with miR-663b mimics and circ_0003215-WT compared to circ_0003215-MUT (right). * P

    Article Snippet: The CRC cell lines (SW620, HCT116, SW480, DLD-1, LOVO, and HT29) and the human embryonic kidney epithelial cell line (HEK-293T) were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Expressing, Agarose Gel Electrophoresis, Quantitative RT-PCR, Incubation, Sequencing, Fluorescence In Situ Hybridization, Luciferase, Plasmid Preparation, Transfection

    Circ_0003215 supresses CRC cell proliferation, invasion and migration. A Schematic illustration of three siRNAs was designed to target the back-splicing junction site of circ_0003215. B Knockdown efficiency of three siRNAs in SW480 and HT29 cells. Si2-circ_0003215 has the highest knockdown efficiency. C Schematic graph of the pLCDH-circ_0003215 plasmid constructs(left). The relative expression of circ_0003215 or MYO9B was detected by RT-qPCR after treatment with empty vector or pLCDH-circ_0003215 in CRC cells(right). D , E The cell proliferative effects of circ_0003215 were evaluated in SW480 and HT29 cells by CCK-8 and EdU assays. F Colony formation assay of SW480 cells transfected with control, circ_0003215 siRNA, vector or pLCDH-circ_0003215. G The effect of circ_0003215 on the migration of SW480 cells was detected by wound healing assay. H , I The effect of circ_0003215 on the migration and invasion of CRC cells were evaluated by transwell assay. Graph shows mean ± SD; * P

    Journal: Cell Death & Disease

    Article Title: N6-methyladenosine modification of circ_0003215 suppresses the pentose phosphate pathway and malignancy of colorectal cancer through the miR-663b/DLG4/G6PD axis

    doi: 10.1038/s41419-022-05245-2

    Figure Lengend Snippet: Circ_0003215 supresses CRC cell proliferation, invasion and migration. A Schematic illustration of three siRNAs was designed to target the back-splicing junction site of circ_0003215. B Knockdown efficiency of three siRNAs in SW480 and HT29 cells. Si2-circ_0003215 has the highest knockdown efficiency. C Schematic graph of the pLCDH-circ_0003215 plasmid constructs(left). The relative expression of circ_0003215 or MYO9B was detected by RT-qPCR after treatment with empty vector or pLCDH-circ_0003215 in CRC cells(right). D , E The cell proliferative effects of circ_0003215 were evaluated in SW480 and HT29 cells by CCK-8 and EdU assays. F Colony formation assay of SW480 cells transfected with control, circ_0003215 siRNA, vector or pLCDH-circ_0003215. G The effect of circ_0003215 on the migration of SW480 cells was detected by wound healing assay. H , I The effect of circ_0003215 on the migration and invasion of CRC cells were evaluated by transwell assay. Graph shows mean ± SD; * P

    Article Snippet: The CRC cell lines (SW620, HCT116, SW480, DLD-1, LOVO, and HT29) and the human embryonic kidney epithelial cell line (HEK-293T) were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Migration, Plasmid Preparation, Construct, Expressing, Quantitative RT-PCR, CCK-8 Assay, Colony Assay, Transfection, Wound Healing Assay, Transwell Assay

    The function of GAS6-AS1 is mediated by miR-370-3p and miR-1296-5p. A – E miR-370-3p and miR-1296-5p mimics suppressed the proliferation, migration and invasion of HT29 cells, whereas miR-370-3p and miR-1296-5p mimics partially offset the promotion effects of GAS6-AS1 on HT29 cells’ proliferation, migration and invasion. F – J miR-370-3p and miR-1296-5p inhibitors promoted the proliferation, migration and invasion of LoVo cells, whereas miR-370-3p and miR-1296-5p inhibitors partially reversed the inhibitory effects of shGAS6-AS1 on LoVo cells’ proliferation, migration and invasion. ** P

    Journal: Journal of Translational Medicine

    Article Title: LncRNA GAS6-AS1 facilitates tumorigenesis and metastasis of colorectal cancer by regulating TRIM14 through miR-370-3p/miR-1296-5p and FUS

    doi: 10.1186/s12967-022-03550-0

    Figure Lengend Snippet: The function of GAS6-AS1 is mediated by miR-370-3p and miR-1296-5p. A – E miR-370-3p and miR-1296-5p mimics suppressed the proliferation, migration and invasion of HT29 cells, whereas miR-370-3p and miR-1296-5p mimics partially offset the promotion effects of GAS6-AS1 on HT29 cells’ proliferation, migration and invasion. F – J miR-370-3p and miR-1296-5p inhibitors promoted the proliferation, migration and invasion of LoVo cells, whereas miR-370-3p and miR-1296-5p inhibitors partially reversed the inhibitory effects of shGAS6-AS1 on LoVo cells’ proliferation, migration and invasion. ** P

    Article Snippet: The human CRC cell lines HT29, LoVo, RKO, SW620, the human normal colon epithelial cells (NCM460), and the human embryo kidney cell line HEK-293T were purchased from the Cell Bank of the Chinese Academy of Sciences and the American Type Culture Collection (ATCC).

    Techniques: Migration

    GAS6-AS1 promotes the proliferation, migration and invasion of CRC cells. A The expression of GAS6-AS1 of the CRC cell lines were detected via qRT-PCR. B After upregulation of GAS6-AS1 in HT29 cell lines, the efficiency was verified via qRT-PCR. C After downregulation of GAS6-AS1 in LoVo cell lines, interference efficiency was verified via qRT-PCR. D After upregulation of GAS6-AS1, CCK8 assay revealed that the proliferation of HT29 cells was significantly enhanced. E After downregulation of GAS6-AS1, CCK8 assay revealed that the proliferation of LoVo cells was significantly decreased. F After upregulation of GAS6-AS1, EdU assay revealed that the proliferation of HT29 cells was significantly enhanced. G After downregulation of GAS6-AS1, EdU assay revealed that the proliferation of LoVo cells was significantly decreased. H – M Overexpression of GAS6-AS1 significantly enhanced the migration H , J and invasion L ability of HT29 cells. Knockdown of GAS6-AS1 significantly suppressed the migration I , K and invasion M ability of LoVo cells. (scale bar: 200 μm for EdU assay, 50 μm for wound healing assay, 100 μm for Transwell assay). * P

    Journal: Journal of Translational Medicine

    Article Title: LncRNA GAS6-AS1 facilitates tumorigenesis and metastasis of colorectal cancer by regulating TRIM14 through miR-370-3p/miR-1296-5p and FUS

    doi: 10.1186/s12967-022-03550-0

    Figure Lengend Snippet: GAS6-AS1 promotes the proliferation, migration and invasion of CRC cells. A The expression of GAS6-AS1 of the CRC cell lines were detected via qRT-PCR. B After upregulation of GAS6-AS1 in HT29 cell lines, the efficiency was verified via qRT-PCR. C After downregulation of GAS6-AS1 in LoVo cell lines, interference efficiency was verified via qRT-PCR. D After upregulation of GAS6-AS1, CCK8 assay revealed that the proliferation of HT29 cells was significantly enhanced. E After downregulation of GAS6-AS1, CCK8 assay revealed that the proliferation of LoVo cells was significantly decreased. F After upregulation of GAS6-AS1, EdU assay revealed that the proliferation of HT29 cells was significantly enhanced. G After downregulation of GAS6-AS1, EdU assay revealed that the proliferation of LoVo cells was significantly decreased. H – M Overexpression of GAS6-AS1 significantly enhanced the migration H , J and invasion L ability of HT29 cells. Knockdown of GAS6-AS1 significantly suppressed the migration I , K and invasion M ability of LoVo cells. (scale bar: 200 μm for EdU assay, 50 μm for wound healing assay, 100 μm for Transwell assay). * P

    Article Snippet: The human CRC cell lines HT29, LoVo, RKO, SW620, the human normal colon epithelial cells (NCM460), and the human embryo kidney cell line HEK-293T were purchased from the Cell Bank of the Chinese Academy of Sciences and the American Type Culture Collection (ATCC).

    Techniques: Migration, Expressing, Quantitative RT-PCR, CCK-8 Assay, EdU Assay, Over Expression, Wound Healing Assay, Transwell Assay

    GAS6-AS1 serves as a ceRNA and sponges miR-370-3p and miR-1296-5p. A Subcellular localization of GAS6-AS1 was detected by qRT-PCR in LoVo cells. B Subcellular localization of GAS6-AS1 in HT29 and LoVo cells determined by RNA-FISH (scale bar: 20 μm). C Fold enrichment of GAS6-AS1 in LoVo. D Enrichment of GAS6-AS1 in LoVo cells transfected with miR-370-3p mimic, miR-1296-5p mimic or miR-NC. E Ago2 protein immunoprecipitated by Ago2 antibody or IgG was meatured by western blot. F miR-370-3p/miR-1296-5p and GAS6-AS1 binding sequences and GAS6-AS1mutation sequences. G The luciferase activities in 293T cells co-transfected with wild-type (WT) or mutant (370Mut/1290Mut) GAS6-AS1 plasmid together with miR-370-3p or miR-1296-5p mimic or miR-NC. H qRT-PCR showed that miR-370-3p and miR-1296-5p level were decreased when GAS6-AS1 overexpressed. I qRT-PCR showed that miR-370-3p and miR-1296-5p level were upregulated when GAS6-AS1 knockdown. ** P

    Journal: Journal of Translational Medicine

    Article Title: LncRNA GAS6-AS1 facilitates tumorigenesis and metastasis of colorectal cancer by regulating TRIM14 through miR-370-3p/miR-1296-5p and FUS

    doi: 10.1186/s12967-022-03550-0

    Figure Lengend Snippet: GAS6-AS1 serves as a ceRNA and sponges miR-370-3p and miR-1296-5p. A Subcellular localization of GAS6-AS1 was detected by qRT-PCR in LoVo cells. B Subcellular localization of GAS6-AS1 in HT29 and LoVo cells determined by RNA-FISH (scale bar: 20 μm). C Fold enrichment of GAS6-AS1 in LoVo. D Enrichment of GAS6-AS1 in LoVo cells transfected with miR-370-3p mimic, miR-1296-5p mimic or miR-NC. E Ago2 protein immunoprecipitated by Ago2 antibody or IgG was meatured by western blot. F miR-370-3p/miR-1296-5p and GAS6-AS1 binding sequences and GAS6-AS1mutation sequences. G The luciferase activities in 293T cells co-transfected with wild-type (WT) or mutant (370Mut/1290Mut) GAS6-AS1 plasmid together with miR-370-3p or miR-1296-5p mimic or miR-NC. H qRT-PCR showed that miR-370-3p and miR-1296-5p level were decreased when GAS6-AS1 overexpressed. I qRT-PCR showed that miR-370-3p and miR-1296-5p level were upregulated when GAS6-AS1 knockdown. ** P

    Article Snippet: The human CRC cell lines HT29, LoVo, RKO, SW620, the human normal colon epithelial cells (NCM460), and the human embryo kidney cell line HEK-293T were purchased from the Cell Bank of the Chinese Academy of Sciences and the American Type Culture Collection (ATCC).

    Techniques: Quantitative RT-PCR, Fluorescence In Situ Hybridization, Transfection, Immunoprecipitation, Western Blot, Binding Assay, Luciferase, Mutagenesis, Plasmid Preparation

    GAS6-AS1 promotes CRC tumorigenesis and metastasis in vivo. A Representative images and the volume of tumors derived from HT29 cells with or without GAS6-AS1 overexpression. B Representative images and the volume of tumors derived from LoVo cells with or without GAS6-AS1 inhibition. C , D The weight of formed tumors. E HT29 cells with or without GAS6-AS1 overexpression were injected into the tail vein of mice to construct lung metastasis models, the representative images and numbers of metastatic nodules in the lungs. F LoVo cells with or without GAS6-AS1 knockdown were injected into the tail vein of mice to construct lung metastasis models, the representative images and numbers of metastatic nodules in the lungs. The tumor micro metastasis nodules in the lungs were counted according to H E staining. (scale bar: 50 μm). ** P

    Journal: Journal of Translational Medicine

    Article Title: LncRNA GAS6-AS1 facilitates tumorigenesis and metastasis of colorectal cancer by regulating TRIM14 through miR-370-3p/miR-1296-5p and FUS

    doi: 10.1186/s12967-022-03550-0

    Figure Lengend Snippet: GAS6-AS1 promotes CRC tumorigenesis and metastasis in vivo. A Representative images and the volume of tumors derived from HT29 cells with or without GAS6-AS1 overexpression. B Representative images and the volume of tumors derived from LoVo cells with or without GAS6-AS1 inhibition. C , D The weight of formed tumors. E HT29 cells with or without GAS6-AS1 overexpression were injected into the tail vein of mice to construct lung metastasis models, the representative images and numbers of metastatic nodules in the lungs. F LoVo cells with or without GAS6-AS1 knockdown were injected into the tail vein of mice to construct lung metastasis models, the representative images and numbers of metastatic nodules in the lungs. The tumor micro metastasis nodules in the lungs were counted according to H E staining. (scale bar: 50 μm). ** P

    Article Snippet: The human CRC cell lines HT29, LoVo, RKO, SW620, the human normal colon epithelial cells (NCM460), and the human embryo kidney cell line HEK-293T were purchased from the Cell Bank of the Chinese Academy of Sciences and the American Type Culture Collection (ATCC).

    Techniques: In Vivo, Derivative Assay, Over Expression, Inhibition, Injection, Mouse Assay, Construct, Staining